Location
D.P. Culp Center Ballroom
Start Date
4-5-2024 9:00 AM
End Date
4-5-2024 11:30 AM
Poster Number
87
Name of Project's Faculty Sponsor
Devapiran Jaishankar, M.D.
Faculty Sponsor's Department
Division of Hematology/Oncology, College of Medicine, East Tennessee State University, Johnson City, TN.
Competition Type
Competitive
Type
Poster Presentation
Presentation Category
Health
Abstract or Artist's Statement
Anemia is commonly seen in alcoholics due to ineffective erythropoiesis, nutritional deficiency, or liver dysfunction. Hemolytic anemia secondary to alcohol use is rare and may mimic Thrombotic microangiopathy (TMA). Early recognition is important as the treatment varies. We present a case of alcohol induced hemolytic anemia mimicking TMA. A 33-year-old male presented to the emergency department with abdominal bloating, swelling in both legs, and weight gain of 30 pounds. He denied vomiting, urinating, or defecating any blood. He had not sought any medical care in the last 15 years. He endorsed daily alcohol consumption, around 12 beers daily for over a decade but denied any drug use except occasional marijuana. Physical examination revealed a petechial rash, mild scleral icterus disproportionate to his bilirubin. Laboratory findings significant for hemoglobin (Hgb) at 6.0 g/dL with a MCV of 115 fL, Platelets 86,000 per uL. Coagulation panel noted prolonged prothrombin time 37.7 seconds and an activated partial thromboplastin time of 44.7 seconds with a low fibrinogen level concerning for disseminated intravascular coagulation (DIC). Factor VIII activity was normal, arguing against DIC. Liver function tests noted elevated total bilirubin at 18.9 mg/dL, predominantly indirect hyperbilirubinemia (16.8 mg/dL), with ALT and AST within normal limits. Reticulocyte count (10.3%) and LDH (572 U/L) were significantly elevated, haptoglobin was low at <30 mg/dL. Direct Coomb’s test was negative. The peripheral smear revealed schistocytes suggesting microangiopathic hemolytic anemia. ADAMTS-13 testing (a disintegrin-like metalloproteinase with thrombospondin motif type 1 member 13) was normal at 96% activity level/function, ruling out thrombotic thrombocytopenic purpura (TTP). Additional work up for paroxysmal nocturnal hemoglobinuria, malignancies of multiple cell lines, Wilson’s disease, and Alpha-1-Antitrypsin deficiency were negative. Due to persistent reticulocytosis (without drop in Hgb), hyperbilirubinemia and impending hepatic failure, the patient was transferred to a comprehensive liver transplantation center for further evaluation and management. Recognizing the etiology of hemolytic anemia is important as the management varies. Alcohol induced hemolytic anemia is a rare entity reported in the literature, first reported by Dr. Zieve. The pathophysiology of alcohol related Coomb’s negative hemolytic anemia is not fully understood. Vitamin E deficiency secondary to alcohol use causing pyruvate kinase instability affects RBC metabolism leading to hemolysis. Management is usually supportive care with alcohol abstinence and transplant if no improvement in hemoglobin and liver function despite abstinence. In conclusion, our case presentation highlights multifactorial anemia commonly seen in patients with alcohol related medical disorders and the need to recognize this rare but potentially dangerous subtype described in the above clinical scenario.
A rare presentation of alcohol induced hemolytic anemia mimicking thrombotic microangiopathy
D.P. Culp Center Ballroom
Anemia is commonly seen in alcoholics due to ineffective erythropoiesis, nutritional deficiency, or liver dysfunction. Hemolytic anemia secondary to alcohol use is rare and may mimic Thrombotic microangiopathy (TMA). Early recognition is important as the treatment varies. We present a case of alcohol induced hemolytic anemia mimicking TMA. A 33-year-old male presented to the emergency department with abdominal bloating, swelling in both legs, and weight gain of 30 pounds. He denied vomiting, urinating, or defecating any blood. He had not sought any medical care in the last 15 years. He endorsed daily alcohol consumption, around 12 beers daily for over a decade but denied any drug use except occasional marijuana. Physical examination revealed a petechial rash, mild scleral icterus disproportionate to his bilirubin. Laboratory findings significant for hemoglobin (Hgb) at 6.0 g/dL with a MCV of 115 fL, Platelets 86,000 per uL. Coagulation panel noted prolonged prothrombin time 37.7 seconds and an activated partial thromboplastin time of 44.7 seconds with a low fibrinogen level concerning for disseminated intravascular coagulation (DIC). Factor VIII activity was normal, arguing against DIC. Liver function tests noted elevated total bilirubin at 18.9 mg/dL, predominantly indirect hyperbilirubinemia (16.8 mg/dL), with ALT and AST within normal limits. Reticulocyte count (10.3%) and LDH (572 U/L) were significantly elevated, haptoglobin was low at <30 mg>/dL. Direct Coomb’s test was negative. The peripheral smear revealed schistocytes suggesting microangiopathic hemolytic anemia. ADAMTS-13 testing (a disintegrin-like metalloproteinase with thrombospondin motif type 1 member 13) was normal at 96% activity level/function, ruling out thrombotic thrombocytopenic purpura (TTP). Additional work up for paroxysmal nocturnal hemoglobinuria, malignancies of multiple cell lines, Wilson’s disease, and Alpha-1-Antitrypsin deficiency were negative. Due to persistent reticulocytosis (without drop in Hgb), hyperbilirubinemia and impending hepatic failure, the patient was transferred to a comprehensive liver transplantation center for further evaluation and management. Recognizing the etiology of hemolytic anemia is important as the management varies. Alcohol induced hemolytic anemia is a rare entity reported in the literature, first reported by Dr. Zieve. The pathophysiology of alcohol related Coomb’s negative hemolytic anemia is not fully understood. Vitamin E deficiency secondary to alcohol use causing pyruvate kinase instability affects RBC metabolism leading to hemolysis. Management is usually supportive care with alcohol abstinence and transplant if no improvement in hemoglobin and liver function despite abstinence. In conclusion, our case presentation highlights multifactorial anemia commonly seen in patients with alcohol related medical disorders and the need to recognize this rare but potentially dangerous subtype described in the above clinical scenario.